ArticlePloS one2013
Elucidation of how cancer cells avoid acidosis through comparative transcriptomic data analysis.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
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- Voltage-gated sodium channels: from roles and mechanisms in the metastatic cell behavior to clinical potential as therapeutic targets.Frontiers in pharmacology · 2023Review
- Flux estimation analysis systematically characterizes the metabolic shifts of the central metabolism pathway in human cancer.Frontiers in oncology · 2023Article
- Importance of lactate dehydrogenase (LDH) and monocarboxylate transporters (MCTs) in cancer cells.Health science reports · 2023Article
- The Role of Chloride Channels in the Multidrug Resistance.Membranes · 2021Review
- Targeting the Interplay between Cancer Metabolic Reprogramming and Cell Death Pathways as a Viable Therapeutic Path.Biomedicines · 2021Review
- Impact of the acidic environment on gene expression and functional parameters of tumors in vitro and in vivo.Journal of experimental & clinical cancer research : CR · 2021Article
- Melatonin regulates tumor aggressiveness under acidosis condition in breast cancer cell lines.Oncology letters · 2019Article
- Overcoming transporter-mediated multidrug resistance in cancer: failures and achievements of the last decades.Drug delivery and translational research · 2019Review
- Crosstalk between the Warburg effect, redox regulation and autophagy induction in tumourigenesis.Cellular & molecular biology letters · 2018Review
- Tumour-specific metabolic adaptation to acidosis is coupled to epigenetic stability in osteosarcoma cells.American journal of cancer research · 2016Article
- Acidosis promotes invasiveness of breast cancer cells through ROS-AKT-NF-κB pathway.Oncotarget · 2014Article
- Microenvironmental acidosis in carcinogenesis and metastases: new strategies in prevention and therapy.Cancer metastasis reviews · 2014Review
- Bicarbonate transport inhibitor SITS modulates pH homeostasis triggering apoptosis of Dalton's lymphoma: implication of novel molecular mechanisms.Molecular and cellular biochemistry · 2014Article
- Inhibition of the vacuolar ATPase induces Bnip3-dependent death of cancer cells and a reduction in tumor burden and metastasis.Oncotarget · 2014Article
- Glycolysis, tumor metabolism, cancer growth and dissemination. A new pH-based etiopathogenic perspective and therapeutic approach to an old cancer question.Oncoscience · 2014Article
- Tumor microenvironmental changes induced by the sulfamate carbonic anhydrase IX inhibitor S4 in a laryngeal tumor model.PloS one · 2014Article
- Cariporide and other new and powerful NHE1 inhibitors as potentially selective anticancer drugs--an integral molecular/biochemical/metabolic/clinical approach after one hundred years of cancer research.Journal of translational medicine · 2013Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The rapid growth of cancer cells fueled by glycolysis produces large amounts of protons in cancer cells, which tri mechanisms to transport them out, hence leading to increased acidity in their extracellular environments. It has been well established that the increased acidity will induce cell death of normal cells but not cancer cells. The main question we address here is: how cancer cells deal with the increased acidity to avoid the activation of apoptosis. We have carried out a comparative analysis of transcriptomic data of six solid cancer types, breast, colon, liver, two lung (adenocarcinoma, squamous cell carcinoma) and prostate cancers, and proposed a model of how cancer cells utilize a few mechanisms to keep the protons outside of the cells. The model consists of a number of previously, well or partially, studied mechanisms for transporting out the excess protons, such as through the monocarboxylate transporters, V-ATPases, NHEs and the one facilitated by carbonic anhydrases. In addition we propose a new mechanism that neutralizes protons through the conversion of glutamate to γ-aminobutyrate, which consumes one proton per reaction. We hypothesize that these processes are regulated by cancer related conditions such as hypoxia and growth factors and by the pH levels, making these encoded processes not available to normal cells under acidic conditions.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.